Anti-inflammatory effects of Gingerenone A through modulation of toll-like receptor signaling pathways

被引:1
|
作者
Ko, Hanbin [1 ]
Kim, Byoung Soo [2 ]
Lee, Ye Eun [1 ]
Choi, Tae Hyun [2 ]
Lee, Younghyun [1 ,3 ]
Youn, Hyung-Sun [1 ,3 ]
Gu, Gyo Jeong [1 ]
机构
[1] Soonchunhyang Univ, Grad Sch, Dept Med Sci, Asan 31538, Chungnam, South Korea
[2] Korea Inst Radiol & Med Sci, Div Appl RI, Seoul 01812, South Korea
[3] Soonchunhyang Univ, Coll Med Sci, Dept Biomed Lab Sci, Asan 31538, Chungnam, South Korea
关键词
Toll-like receptor signaling; Gingerenone A; MyD88-dependent pathway; TRIF-Dependent pathway; Anti-inflammation; NITRIC-OXIDE; SUPPRESSION; INHIBITION; ACTIVATION; EXPRESSION; TBK1;
D O I
10.1016/j.ejphar.2024.176997
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Toll-like receptors (TLRs) play a pivotal role in initiating immune responses, particularly in the context of inflammation. However, an excessive inflammation can detrimentally affect the immune homeostasis Thus, it is important to regulate TLR signaling pathways appropriately. Gingerenone A (GIA), a bioactive compound derived from ginger, has garnered significant attention due to its potential anti-inflammatory properties. In this study, we investigate modulatory effects of GIA on TLR signaling pathways. Results showed that GIA effectively suppressed TLR-mediated inflammatory responses by modulating key signaling molecules such as nuclear factor kappa B and interferon regulatory factor 3. These results indicate that GIA is a novel regulator of TLR signaling, offering promising avenues for the development of new anti-inflammatory agents.
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收藏
页数:9
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